The prevalence of diabetes is increasing, particularly in developing regions of the world, including Middle Eastern Countries. The social and economic consequences of this disease and its complications are enormous. The objective is to discuss the scope and implications of the increasing burden of diabetes and describe the rationale and design of a new international study examining blood pressure lowering and glucose control interventions aimed at reducing the risk of vascular complications in people with type 2 diabetes.
Diabetes mellitus is a group of chronic metabolic disorders culminating in the elevation of blood glucose levels due to defective insulin secretion, action or both. Diabetes causes both, microvascular diseases (blindness, kidney failure and nerve damage) caused by damage to small blood capillaries, and macrovascular (stroke and coronary heart disease) caused by atherosclerosis.
Insulin is produced in the pancreas and enables cells to absorb glucose and subsequently convert it into energy. Failure to produce or properly respond to it leads to accumulation of glucose in the blood, which further leads to various complications (Tierney, McPhee, and Papadakis, 2002).
Also known as type I diabetes, juvenile diabetes and diabetes mellitus. (Condition: Insulin dependent Diabetes mellitus, 2008)
IDDM is caused by a reaction caused in the body such that the immune system looses the capability of insulin-secreting cells in the pancreas.
Type 2 diabetes has a long asymptomatic phase and significant clinical risk markers (Caterson 2005).
The decreased ability of insulin to act effectively on peripheral target tissues especially muscle and liver is a prominent feature of type 2 DM, and this is presumed to result from a combination of genetic susceptibility and obesity.
Incretin mimetics like exenatide and liraglutide mimic the action of incretin hormones (glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP)), which are found in the gastrointestinal tract and function in insulin secretion. Dipeptidyl peptidase (DPP-IV) inhibitors like sitagliptin and vildagliptin suppress the degradation of the incretins, thus extending their action.
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